test Browse by Author Names Browse by Titles of Works Browse by Subjects of Works Browse by Issue Dates of Works

Advanced Search
& Collections
Issue Date   
Sign on to:   
Receive email
My Account
authorized users
Edit Profile   
About T-Space   

T-Space at The University of Toronto Libraries >
School of Graduate Studies - Theses >
Master >

Please use this identifier to cite or link to this item: http://hdl.handle.net/1807/29622

Title: Mechanism of MicroRNA miR-520g Pathogenesis in CNS-PNET
Authors: Shih, J. H. David
Advisor: Huang, Annie
Department: Laboratory Medicine and Pathobiology
Keywords: microRNA
brain tumour
cell cycle
Issue Date: 25-Aug-2011
Abstract: We recently discovered a high-level amplicon spanning the chr19q13.41 microRNA cluster in CNS Primitive Neuroectodermal Tumour, which results in striking upregulation of miR-520g. Constitutive over-expression of miR-520g in untransformed human neural stem cells enhanced cell growth, restricted differentiation down the neuronal lineage, and promoted expression of neural stem/progenitor cell markers. We thus hypothesize that ectopic miR-520g expression promotes tumourigenesis in part by inhibiting cellular differentiation. Consistent with this proposition, miR-520g is silenced upon embryonic stem cell differentiation and its expression is absent from most adult tissues. Moreover, expression analysis of miR-520g overexpressing cells revealed significant dysregulation of developmental signalling pathways. Further efforts focused on elucidating mechanisms of miR-520g function led to the identification of a cell cycle inhibitor, p21, as an important candidate target. These findings collectively suggest that miR-520g may modulate differentiation by regulating developmental signalling pathways and cell cycle exit of neural stem/progenitor cells.
URI: http://hdl.handle.net/1807/29622
Appears in Collections:Master

Files in This Item:

File Description SizeFormat
Shih_J_H_David_201103_MSc_thesis.pdf1.43 MBAdobe PDF

This item is licensed under a Creative Commons License
Creative Commons

Items in T-Space are protected by copyright, with all rights reserved, unless otherwise indicated.